SUPPRESSION OF DEVELOPMENT OF EXPERIMENTAL AUTOIMMUNE-THYROIDITIS BY ORAL-ADMINISTRATION OF THYROGLOBULIN

Experimental autoimmune thyroiditis (EAT), which to some extent repres ents an experimental model of human chronic lymphocytic thyroiditis, i s an organ-specific autoimmune disease characterized by autoantibody p roduction to thyroid antigens (Ag) and mononuclear infiltration of the thyroid gland. EAT induced by immunization with human thyroglobulin ( hTG) with Freund's adjuvant in CBA/J (H-2(K)) mice is associated with prominent B and T cell responses. We report that oral administration o f hTG effectively reduces the immune responses in EAT in mice in an Ag -specific manner. Both cellular and humoral immune responses are reduc ed in a dose-dependent manner. Histological evidence of disease is dra matically reduced. Suppression of the immune responses is seen 2 weeks after Ag challenge, with partial inhibition of proliferative and anti body responses. Six weeks after immunization, further inhibition is ob served of both T and B cell responses. Hyporesponsiveness of T and B c ell reactivity is seen only to hTG; T and B cell responses to other im munogens are not affected, including purified protein derivative and t he nonrelated Ag BSA. This model may provide the basis for immunothera py of autoimmune thyroid diseases in man.